Neonatal Hypoglycaemia - Medical Negligence Solicitors – Compensation Claims

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Neonatal Hypoglycemia

Glucose is one of the main sources of energy in the prenatal period and in the neonatal period. Organ and brain function depends on glucose. Because the brain does not carry glycogen stores to any degree, there must be a constant source of glucose to keep the brain going. There is a high brain to body weight so that cerebral glucose accounts for up to 90 percent of glucose consumption.

Glucose is a major source of foetal nutrition. The foetal source of glucose is almost exclusively from the mother with the enzymes to create glucose dormant in the foetus. Glucose is reduced into CO2 and carbon from about 60-70 percent of the utilization of glucose.

While the foetus is dependent on glucose almost entirely, a switch happens upon birth so that the foetus can create glucose and store glucose on its own. There is a decrease in the insulin to glucose ratio so that glucose rises. Infants can create gluconeogenesis by the sixth hour of life, although full enzyme activity doesn’t happen until 1-2 weeks of age. In neonatal hypoglycaemia, the blood glucose goes too low.

The incidence of neonatal hypoglycaemia is from 1-5 out of every 1,000 live births but is about 8 percent for children born to diabetics and 15 percent of all preterm infants. Those with multiple risk factors can have neonatal hypoglycaemia as high as 30 percent. Upon the birth, the diagnosis of neonatal hypoglycaemia is made when the sugar is lower than 35 mg/dL. Concentrations among different paediatricians include levels as low as 20 mg/dL or as high as 70 mg/dL. These are the levels within the first 72 hours of life. The condition is made possible when the glucose delivery is poor and not enough to meet up with demands. It is estimated that a sustained level of less than 20 mg/dL can cause brain damage within a few hours.

The normal blood sugar as a newborn would be considered hypoglycaemic at 18 hours of age. This is why nursing staff frequently check the glucose level in the first few days of life.

The presentation of neonatal hypoglycaemia can be tachypnea, respiratory distress, lack of breathing, shakiness and jitteriness, tachycardia, bradycardia, poor suck, temperature dysregulation, seizures and lethargy. These signs can mimic sepsis, low calcium and intracranial haemorrhage so that further evaluation needs to be made when such symptoms come along.

Causes of neonatal hypoglycaemia include being premature and having intrauterine growth restriction. In both cases, there is a low amount of liver-stored glycogen. In some cases, multiple gestations or post-term infants can suffer from the condition. When there has been increased metabolic use as in a difficult delivery, there can be low blood sugar after birth.

Cases of hyperinsulinism can result in low blood sugar. This happens when a woman who is diabetic delivers an infant. The infant has high blood insulin levels with a sudden drop in serum glucose at birth. The baby suffers from prolonged blood sugar problems and impaired glycogenolysis and gluconeogenesis.

Infants who are born with erythroblastosis foetalis have higher than normal insulin levels. The same is true of infants who were maintained in utero on beta agonist tocolytics medication. This gradually wears off as the tocolytics is washed from the system. Infants with hyperinsulinism can have their symptoms last as long as 4 weeks after the birth.

Management of neonatal hypoglycaemia includes rapid feeding enterally. It should be done with 5 percent dextrose water because it is rapidly metabolized, bringing up the glucose quickly. Only later is formula started. In symptomatic patients, it is recommended to try IV glucose therapy, especially for the sickest babies.

The biggest complication includes the hypoglycaemic brain injury. This can happen when the patient is under-treated during his or her early life.

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